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spineneuro

Surgical Solutions on a Budget: Brain Tumor Surgery Cost in India Demystified - 0 views

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brain tumor surgery cost brain tumor surgery brain tumor surgeons brain tumor surgery hospital

shared by spineneuro on 19 Nov 23 - No Cached
  • spineneuro on 19 Nov 23
     
    The brain tumor surgery cost is exceptionally affordable, with a price nearly one-third of that in developed countries like the US and the UK. In addition to the brain tumor surgery cost, the success rate of the procedure performed by the best doctors for brain cancer in India is comparable to some of the best brain tumor surgery hospitals globally.
spineneuro

Artificial Intelligence Expedites Brain Tumor Diagnosis during Brain Tumor Surgery in W... - 0 views

www.101pressrelease.com/g-brain-tumor-surgery-in-world

brain tumor surgeons in world Top 10 brain tumor surgeons in world best brain tumor surgery in world brain tumor

shared by spineneuro on 31 Jan 22 - No Cached
  • spineneuro on 31 Jan 22
     
    Before the new technology may be elevated to different centers and institutions, "robust testing with more patients and increasing the generation to include rare brain tumors are substantially needed," Top 10 brain tumor surgeons in world said.
Nathan Goodyear

Anti-helminth compound niclosamide downregulates Wnt Signaling and elicits antitumor re... - 0 views

www.ncbi.nlm.nih.gov/...PMC3117125

Niclosamide Wnt cancer colon cancer

shared by Nathan Goodyear on 21 Mar 18 - No Cached
  • Others have reported that niclosamide inhibits the NF-κB pathway in leukemia cell lines (26) or mTOR signaling in MCF-7 breast cancer cells
  • niclosamide enhances the anti-tumor effect of oxaliplatin
  • In the more rapidly growing tumor (HCT116), a dose of 200 mg/kg of body weight was needed to suppress the tumor growth
  • ...13 more annotations...
  • however, 100 mg/kg of niclosamide could suppress the growth of the relatively slow-growing tumor (CRC039) to the same level
  • niclosamide was confirmed to inhibit the growth of human CRCs in NOD/SCID mice
  • niclosamide can inhibit Wnt pathway activation in CRC
  • The mechanism of action of the niclosamide in our studies is thought to be through internalization of Fzd1 and downregulation of Wnt pathway intermediaries
  • Recently, Jin et al. (26) reported that niclosamide inhibited the NF-κB pathway and increased reactive oxygen species levels to induce apoptosis in AML cells. In contrast, we did not observe any inhibitory effect of niclosamide on NF-κB signaling in our CRC model
  • oral administration of niclosamide does result in sufficient distribution of the drug into tumor tissue, to prove a prolonged inhibitory effect on Wnt/ß-catenin signaling, resulting in tumor growth inhibition
  • we required higher doses (100 ~ 200 mg/kg body weight) of niclosamide in order to demonstrate significant inhibition of tumor growth in NOD/SCID mice
  • niclosamide concentrations in tumor tissue showed good correlation with those in plasma, suggesting the efficient distribution of niclosamide from blood to tumor tissue
  • we observed downregulation of Dvl2 and ß-catenin cytosolic expression in niclosamide-treated tumor cells in vivo
  • One potential concern for the use of niclosamide as an anticancer therapy is the poor absorption of this drug
  • The Wnt signaling pathway, fundamental to embryonic tissue patterning, is also activated in stem-like cells
  • The canonical Wnt pathway is activated in approximately 80% of sporadic CRC primarily due to mutations in the APC gene
  • recent observations reveal that Wnt ligands or inhibitors may affect the growth and survival of colon cancer cells in spite of the presence of APC or CTNNB1 mutations
  • Nathan Goodyear on 21 Mar 18
     
    Niclosamide found to inhibit Wnt/B-catenin signaling pathway, and thus promotion of apoptosis, in colorectal cancer cells in Vivo study.  It was also found to augment chemotherapeutic.
spineneuro

Health Articles - Brain Tumor Surgery Cost in India Is As Good As Anywhere Else in the... - 0 views

www.amazines.com/...6262353

Brain Tumor Surgery in India Brain Tumor Surgery Cost India Cost of Brain Tumor Surgery India Top Brain Tumor Surgeons India Best Brain Tumor Surgeons of India List of Top Brain Tumor Surgeons India

shared by spineneuro on 23 Aug 21 - No Cached
  • spineneuro on 23 Aug 21
     
    Brain tumor surgery cost India, it is extraordinarily affordable and when compared to the developed countries comes out to be extraordinarily low cost, which is nearly one third the price in evaluation to US & UK.Top brain tumor surgeon India have gained reputation all across the world, all thanks to the high end specialists giving the best of the healthcare service at affordable cost.Spine and neuro surgery service India is right here that will help you with the high-quality low cost medical neurology procedure. Please Call +91-98604-32255 Email id:- enquiry@spineandneurosurgeryhospitalindia.co
spineneuro

The Cost-Effective Solution: Affordable Brain Tumor Surgery in India - 0 views

www.linkedin.com/...ain-tumor-india-hospital-india

Brain tumor surgery cost Brain tumor surgery affordable brain tumor surgery cost

shared by spineneuro on 24 Apr 23 - No Cached
  • spineneuro on 24 Apr 23
     
    Brain tumor surgery cost, its miles distinctly affordable and when in comparison to the evolved countries comes out to be tremendously low price, which is almost one 1/3 the rate in evaluation to US & UK. Besides the cost, the success rate of the process by a list of top brain tumor surgeons in India is at par globally with some of the brain tumor surgery best hospitals in India.
spineneuro

Get New-Age Technology and Expertise At Top Hospitals for Brain Tumor India - Spine and... - 0 views

spineandneurosurgeryhospitalindia.wordpress.com/...ospitals-for-brain-tumor-india

brain tumor surgery top brain tumor hospitals in India Top Brain Tumor Surgeon In India

shared by spineneuro on 08 Jun 22 - No Cached
  • spineneuro on 08 Jun 22
     
    It is been observed that brain tumor surgery in India is around 60% lesser than in other western advanced countries. That is why overseas patients choose India for their brain tumor surgery because of professional surgeons, top brain tumor hospitals in India, and affordable cost.
Nathan Goodyear

The impact of the microbiome in cancer: Targeting metabolism of cancer cells and host -... - 0 views

www.ncbi.nlm.nih.gov/...PMC9708872

tumor microbiome cancer gut microbiome TME metabolism

shared by Nathan Goodyear on 20 Mar 24 - No Cached
  • Nathan Goodyear on 20 Mar 24
     
    Studies have found that high-salt diet can enhance the function of natural killer (NK) cells by enriching the abundance of Bifidobacterium, thus inhibiting tumor growth (63). High dietary fiber can enrich A. muciniphila, activate innate immunity, reshape the tumor microenvironment, and exert the function of inhibiting tumor (64). Notably, Wargo et al. have confirmed that high-dietary fiber diet can enhance anti-tumor immunity and increase the infiltration of tumor-killing T cells, while commercial probiotics treatment alone does not enhance the efficacy of immunotherapy. This study suggests that probiotics intervention is strain-specific and should be put in a specific dietary environment to make sense, to some extent (65).
Nathan Goodyear

Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor,... - 0 views

europepmc.org/...PMC2510818

GC-MAF Nagalase cancer prostate cancer immunotherapy PSA

shared by Nathan Goodyear on 08 May 18 - No Cached
  • the MAF precursor activity of prostate cancer patient Gc protein is lost or reduced, because their serum Gc protein is deglycosylated by serum α-N-acetylgalactosaminidase (Nagalase) secreted from cancerous cells
  • Administration of 100 ng of GcMAF
  • 100 ng of GcMAF was administered intramuscularly once a week
  • ...11 more annotations...
  • As GcMAF therapy progressed the MAF precursor activity of all five patients increased and their serum Nagalase activity decreased inversely
  • As GcMAF therapy progressed, the MAF precursor activity increased with a concomitant decrease in serum Nagalase activity
  • serum Nagalase is proportional to tumor burden
  • as GcMAF therapy progressed, serum Nagalase activity decreased and, concomitantly, tumor burden decreased
  • the serum Nagalase activities of all 16 patients decreased as GcMAF therapy progressed
  • annual computed tomographic scans of these patients confirmed them being tumor recurrence-free for the 7 years
  • undifferentiated cells were killed rapidly during the first few weeks, and the differentiated cells were killed slowly in the remaining GcMAF therapeutic period
  • PSA levels of prostatectomized patients decreased as serum Nagalase decreased during GcMAF therapy
  • In patients without tumor resection, however, although serum Nagalase activity decreased as GcMAF therapy progressed, their PSA values remained unchanged. The result suggests that the PSA derived from tumor-bearing prostate did not change while tumor burden decreased. Because tumor-induced inflammation in the noncancerous prostate tissues causes secretion of PSA [38], the PSA produced from these inflamed noncancerous prostate tissues cannot be changed by the decrease in tumor burden
  • Advanced cancer patients have high serum Nagalase activities, resulting in no macrophage activation and severe immunosuppression that explain why cancer patients die with overwhelming infection
  • Prognostic utility of serum α-N-acetylgalactosaminidase and immunosuppression resulted from deglycosylation of serum Gc protein in oral cancer patients
  • Nathan Goodyear on 08 May 18
     
    GC-MAF levels exist in inverse relationship to nagalase.  In this study of men with prostate cancer, weekly GCMAF injections reduced Nagalase activity to levels found in healthy controls suggesting tumor free. The dose was 100 ng/week. Nagalase is a protein that suppresses GC-MAF production and thus is immunosuppressive.
Nathan Goodyear

Curcumin Down-Regulates DNA Methyltransferase 1 and Plays an Anti-Leukemic Role in Acut... - 0 views

www.ncbi.nlm.nih.gov/...PMC3572185

aml acute myeloid leukemia cancer leukemia curcumin NF-kappaB

shared by Nathan Goodyear on 12 May 18 - No Cached
  • In a variety of solid tumors and blood cancers, aberrant hypermethylation of CpG-rich regions (>55% CG content, 0.5-4 kb in length, the so-called “CpG islands”) in the promoters of tumor suppressor genes (TSGs) results in their transcriptional silencing
  • These agents have been reported to suppress tumor growth by reversing aberrantly hypermethylation in the promoters of inactivated TSGs (e.g. p15INK4B), allowing re-expression of TSGs, thereby restoring normal cell cycle regulation, proliferation, apoptosis, and differentiation
  • groups have reported that curcumin acts as a scavenger of free radicals [13], an inhibitor of NF-κB nuclear translocation [14], and a modulator of histone deacetylase (HDAC) and histone acetyltransferase (HAT)
  • ...9 more annotations...
  • In this study, we found that curcumin down-regulated DNMT1 expression in AML cells. This occurred, at least in part, through down-modulation of two positive regulators of DNMT1: Sp1 and the NF-κB component, p65. We also found that curcumin-mediated down-regulation of DNMT1 was associated with reactivation of TSGs and tumor suppression, both in vivo and in vitro.
  • curcumin may selectively downregulate DNMT1 expression in tumor cells, but not in normal cells
  • DNMT1 expression is positively regulated by Sp1 and the NF-κB signaling component
  • indicating that curcumin may have significant anti-tumor activity in AML
  • We found that, compared to the vehicle control, curcumin treatment reduced tumor weight by 70%
  • Surprisingly, although curcumin significantly inhibited tumor growth in these mice, we were unable to find any obvious toxicity associated with curcumin treatment
  • Consistent with our observations regarding curcumin’s ability to inhibit tumor growth in vivo (Figure 4) and down-regulate DNMT1 expression in vitro and ex vivo (Figure 1), we found that decreased levels of DNMT1 protein and mRNA were expressed by tumor cells isolated from curcumin-treated mice
  • we identified curcumin as a substance which acts as an inhibitor of DNA methyltransferase enzymatic activity and induces significant global DNA hypomethylation in AML cells
  • In this study, we first demonstrated that curcumin decreases DNMT1 mRNA and protein expression levels, most likely through inhibiting expression of positive regulators of DNMT1, such as Sp1 and the p65 component of NF-κB component, and/or altering their ability to bind to the promoter region of DNMT1
  • Nathan Goodyear on 12 May 18
     
    Curcumin beneficial in AML
Nathan Goodyear

Clinical experience with intravenous administration of ascorbic acid: achievable levels... - 0 views

www.ncbi.nlm.nih.gov/...PMC3751545

IV vitamin C dosing ascorbic acid inflammation disease cancer IV vitamin C intravenous vitamin C IV intravenous vitamin C vitamin C CRP therapy treatment alternative

shared by Nathan Goodyear on 26 Aug 14 - No Cached
  • Patients with higher tumor markers are likely to have higher tumor burden, higher oxidative stress and, therefore, are more likely to have lower post IVC plasma levels.
  • Our data also showed that cancer patients with metastasis tend to have lower post-IVC vitamin C levels than those without metastasis
  • Lower peak plasma concentrations are obtained in cancer patients than in healthy subjects. Cancer patients who are deficient in vitamin C prior to therapy tend to achieve lower plasma levels post infusion.
  • ...25 more annotations...
  • Patients with higher inflammation or tumor burdens, as measured by CRP levels or tumor antigen levels, tend to show lower peak plasma ascorbate levels after IVC.
  • Patients with metastatic tumors tend to achieve lower post infusion plasma ascorbate levels than those with localized tumors.
  • Meta-analyses of clinical studies involving cancer and vitamins also conclude that antioxidant supplementation does not interfere with the efficacy of chemotherapeutic regiments
  • Most of the prostate cancer patients studied, 75±19% (95% confidence), showed reductions in PSA levels during the course of their IVC therapy
  • Laboratory studies suggest that, at high concentrations, ascorbate does not interfere with chemotherapy or irradiation and may enhance efficacy in some situations
  • Cameron and Pauling observed fourfold survival times in terminal cancer patients treated with intravenous ascorbate infusions followed by oral supplementation
  • The inflammatory microenvironment of cancer cells leads to increasing oxidative stress, which apparently depletes vitamin C, resulting in lower plasma ascorbate concentrations in blood samples post IVC infusion. Another explanation for this finding may be that cancers are themselves more metabolically active in their uptake of vitamin C, causing subjects to absorb more of the vitamin, and as a results show lower plasma ascorbate concentrations in blood post IVC infusion.
  • patients with severely elevated CRP levels attain plasma ascorbate concentrations after IVC infusions that are only 65% of those attained for subjects with normal CRP levels
  • The finding of decreased plasma ascorbate levels in cancer patients may relate to the molecular structure of ascorbic acid; in particular, the similarity of its oxidized form, dihydroascorbic acid, to glucose
  • Since tumor have increased requirement for glucose [67], transport of dehydroascorbate into the cancer cells via glucose transport molecules and ascorbate through sodium-dependent transporter may be elevated
  • Increased accumulation of ascorbic acid in the tumor site was supported by measurements of the level of ascorbic acid in tumors in animal experiments
  • patients with advanced malignancies may have lower level of ascorbic acid in tissue, creating a higher demand for the vitamin C
  • IVC therapy appears to reduce CRP levels in cancer patients.
  • CRP concentrations directly correlate with disease activity in many cases and can contribute to disease progression through a range of pro-inflammatory properties.
  • Being an exquisitely sensitive marker of systemic inflammation and tissue damage, CRP is very useful in screening for organic disease and monitoring treatment responses
  • ncreases in CRP concentrations have been associated with poorer prognosis of survival in cancer patients, particularly with advance disease independent of tumor stage
  • Regarding inflammation, 73±13% of subjects (95% confidence) showed a reduction in CRP levels during therapy. This was an even more dramatic 86±13% (95% confidence) in subjects who started therapy with CRP levels above 10 mg/L
  • patients treated by IVC with follow-up several year showed that suppression of inflammation in cancer patients by high-dose IVC is feasible and potentially beneficial
  • Inflammation is a marker of high cancer risk, and poor treatment outcome
  • The subjects with highly elevated CRP concentrations have a three-fold elevation “all-cause” mortality risk and a twenty-eight fold increase in cancer mortality risk
  • cancer patients may need higher doses to achieve a given plasma concentration.
  • patients with lower vitamin C levels may see more distribution of intravenously administered ascorbate into tissues and thus attain less in plasma.
  • When treating patients with IVC, the first treatment likely serves to replenish depleted tissue stores, if those subjects were vitamin C deficient at the beginning of the treatment. Then, in subsequent treatments, with increasing doses, higher plasma concentrations can be attained. On-going treatments serve to progressively reduce oxidative stress in cancer patients.
  • large doses given intravenously may result in maximum plasma concentrations of roughly 30 mM, a level that has been shown to be sufficient for preferential cytotoxicity against cancer cells
  • oral intake of vitamin C exceeded 200 mg administered once daily, it was difficult to increase plasma and tissue concentrations above roughly 200 μM.
  • Nathan Goodyear on 26 Aug 14
     
    Great review on the use of IV vitamin C in cancer and to reduce inflammation.  The article does a great job of discussing the mechanism of vitamin C therapy in cancer as well as the proposed reasons for low vitamin C in cancer patients.  The study also highlights the obstacles to rise in vitamin C levels post IV vitamin C in cancer patients.
Nathan Goodyear

Therapeutic hyperthermia: The old, the new, and the upcoming - Critical Reviews in Onco... - 1 views

www.croh-online.com/...fulltext

hyperthermia hyperthermic therapy cancer oncology

shared by Nathan Goodyear on 30 Aug 18 - No Cached
  • not well understood, but it is felt to be a combination of both heat-induced necrosis and of protein inactivation (e.g., repair enzymes) as opposed to DNA damage
  • alterations in tumor cytoskeletal and membrane structures, which disrupt cell motility and intracellular signal transduction
  • A common explanation for HT-enhancement of RT and CT involves inhibition of homologous recombination repair of double-strand DNA breaks, preventing cells from repairing sub-lethal damage
  • ...15 more annotations...
  • it does appear to inhibit rejoining of RT-induced DNA breaks more than is commonly observed after RT alone
  • HT damages cells and enhances RT and CT sensitivity as a function of both temperature and duration of treatment
  • as temperature or duration increase, the rate of cell killing also increases
  • At temperatures above 42 °C, tumor vasculature is damaged, resulting in decreased blood flow
  • Cancer cells are particularly vulnerable to heating; in vivo studies have shown that temperatures in the range of 40–44 °C cause more selective damage to tumor cells
  • cancerous blood vessels are chaotic, leaky, and inefficient
  • selective cytotoxic effect on tumor cells include inhibition of key cancer cell-signaling pathways such as AKT, inducing apoptosis, suppression of cancer stem cell proliferation, and others
  • increase in immunological attacks against tumors after HT, which were believed to be achieved through activation of HSPs and subsequent modulation of the innate and adaptive immune responses against tumor cells
  • HT does lead to activation of the immune system and HSP-induced cell death through modification of the tumor cell surface
  • These HSPs and tumor antigens are taken up by dendritic cells and macrophages and go on to induce specific anti-tumor immunity
  • In vivo studies demonstrate HT-enhancement of NK cell activity, and HT has been shown to increase neutrophilic granulocytes with anti-tumor activity
  • it has become increasingly clear that HT results in immune stimulation, through both direct heat-mediated cell killing as well as innate and adaptive immune system modulation
  • The term hyperthermia is used in this review to refer to heating within the clinically accepted range of 40–45 °C
  • temperatures above 42.5–43 °C the exposure time can be halved with each 1 °C increase while maintaining equivalent cell killing
  • gradual heating at 43 °C for 1 h worked through an apoptotic pathway
  • Nathan Goodyear on 30 Aug 18
     
    Comprehensive review of hyperthemic therapy.
spineneuro

Get the Most Reliable Care With Brain Tumor Surgery In India - 0 views

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brain tumor brain tumor surgery Brain tumor surgery cost Brain tumor surgeon

shared by spineneuro on 07 Nov 22 - No Cached
  • spineneuro on 07 Nov 22
     
    A brain tumor is known as an unusual mass of cells in the brain that have no reason. In general, tumors arise while cells divide and grow excessively within the body.
spineneuro

Never Give Up Hope With Top 5 Brain Tumor Surgeons in World - Spine and Neuro Hospital ... - 0 views

spineandneurosurgeryhospitalindia.wordpress.com/...-brain-tumor-surgeons-in-world

brain tumor brain surgery brain tumor removal surgery cost brain tumor surgeons tumor

shared by spineneuro on 15 Feb 22 - No Cached
  • spineneuro on 15 Feb 22
     
    It is been observed that affordable brain tumor removal surgery cost in India is around 60% lesser than other western advanced countries. Brain tumor removal surgery cost in India is extraordinarily affordable and when compared to the developed countries comes out to be extraordinarily low cost, which is nearly one-third of cost in evaluation to US & UK. Call us at +91-98604-32255 or Mail us at: enquiry@spineandneurosurgeryhospitalindia.com
spineneuro

Get Superior Brain Tumor Surgery in India on Behance - 0 views

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Brain Tumor Surgery brain tumor surgery success rate in India common symptoms For Brain Tumor Surgery brain tumor surgery cost in rupees

shared by spineneuro on 16 Mar 22 - No Cached
  • spineneuro on 16 Mar 22
     
    That is true for people undergoing brain tumor surgery in India, even as in most cases, the patients in the preliminary levels in their cancer get effortlessly cured with high brain tumor surgery success rate in India. Although success rates offered are more than 98%, patients are usually satisfied with the surgical result. Send Your Medical Report by Email at: enquiry@spineandneurosurgeryhospitalindia.com or you can Talk with our Expert in Call just dial +91-9325887033
Nathan Goodyear

The river blindness drug Ivermectin and related macrocyclic lactones inhibit WNT-TCF pa... - 0 views

www.ncbi.nlm.nih.gov/...PMC4287931

ivermectin cancer WTF Selamectin

shared by Nathan Goodyear on 19 Mar 18 - No Cached
  • WNT signaling
  • early colon cancers commonly display loss of function of the tumor suppressor Adenomatous polyposis coli (APC), a key component of the β-CATENIN destruction complex
  • Other cancers also show an active canonical WNT pathway; these include carcinomas of the lung, stomach, cervix, endometrium, and lung as well as melanomas and gliomas
  • ...31 more annotations...
  • In normal embryogenesis and homeostasis, the canonical WNT pathway is activated by secreted WNT ligands produced in highly controlled context-dependent manners and in precise amounts. WNT activity is transduced in the cytoplasm, inactivates the APC destruction complex, and results in the translocation of activate β-CATENIN to the nucleus, where it cooperates with DNA-binding TCF/LEF factors to regulate WNT-TCF targets and the ensuing genomic response
  • beyond the loss of activity of the APC destruction complex, for instance throughAPC mutation, phosphorylation of β-CATENIN at C-terminal sites is required for the full activation of WNT-TCF signaling and the ensuing WNT-TCF responses in cancer.
  • The WNT-TCF response blockade that we describe for low doses of Ivermectin suggests an action independent to the deregulation of chloride channels
  • involve the repression of the levels of C-terminally phosphorylated β-CATENIN forms and of CYCLIN D1, a critical target that is an oncogene and positive cell cycle regulator.
  • the Avermectin single-molecule derivative Selamectin, a drug widely used in veterinarian medicine (Nolan & Lok, 2012), is ten times more potent acting in the nanomolar range
  • Ivermectin also diminished the protein levels of CYCLIN D1, a direct TCF target and oncogene, in both HT29 and H358 tumor cells
  • Activated Caspase3 was used as a marker of apoptosis by immunohistochemistry 48 h after drug treatment. Selamectin and Ivermectin induced up to a sevenfold increase in the number of activated Caspase3+ cells in two primary (CC14 and CC36) and two cell line (DLD1 and Ls174T) colon cancer cell types (Fig​(Fig2C).2C). All changes were significative
  • The strong downregulation of the expression of the intestinal stem cell genesASCL2 andLGR5 (van der Flieret al, 2009; Scheperset al, 2012; Zhuet al, 2012b) by Ivermectin and Selamectin (Fig​(Fig2D)2D) raised the possibility that these drugs could affect WNT-TCF-dependent colon cancer stem cell behavior
  • Pre-established H358 tumors responded to Ivermectin showing a ˜ 50% repression of growth
  • Ivermectin hasin vivo efficacy against human colon cancer xenografts sensitive to TCF inhibition with no discernable side effects
  • Ivermectin (Campbellet al, 1983), an off-patent drug approved for human use, and related macrocyclic lactones, have WNT-TCF pathway response blocking and anti-cancer activities
  • these drugs block WNT-TCF pathway responses, likely acting at the level of β-CATENIN/TCF function, affecting β-CATENIN phosphorylation status.
  • anti-WNT-TCF activities of Ivermectin and Selamectin
  • Ivermectin has a well-known anti-parasitic activity mediated via the deregulation of chloride channels, leading to paralysis and death (Hibbs & Gouaux, 2011; Lynagh & Lynch, 2012). The same mode of action has been suggested to underlie the toxicity of Ivermectin for liquid tumor cells and the potentiation or sensitization effect of Avermectin B1 on classical chemotherapeutics
  • the specificity of the blockade of WNT-TCF responses we document, at low micromolar doses for Ivermectin and low nanomolar doses for Selamectin, indicate that the blockade of WNT-TCF responses and chloride channel deregulation are distinct modes of action
  • What is key then is to find a dose and a context where the use of Ivermectin has beneficial effects in patients, paralleling our results with xenografts in mice.
  • Cell toxicity appears at doses greater (> 10 μM for 12 h or longer or > 5 μM for 48 h or longer for Ivermectin) than those required to block TCF responses and induce apoptosis.
  • Our data point to a repression of WNT-β-CATENIN/TCF transcriptional responses by Ivermectin, Selamectin and related macrocylic lactones.
  • (i) The ability of Avermectin B1 to inhibit the activation of WNT-TCF reporter activity by N-terminal mutant (APC-insensitive) β-CATENIN as detected in our screen
  • (ii) The ability of Avermectin B1, Ivermectin, Doramectin, Moxidectin and Selamectin to parallel the modulation of WNT-TCF targets by dnTCF
  • (iii) The finding that the specific WNT-TCF response blockade by low doses of Ivermectin and Selamectin is reversed by constitutively active TCF
  • (iv) The repression of key C-terminal phospho-isoforms of β-CATENIN resulting in the repression of the TCF target and positive cell cycle regulator CYCLIN D1 by Ivermectin and Selamectin
  • (v) The specific inhibition ofin-vivo-TCF-dependent, but notin-vivo-TCF-independent cancer cells by Ivermectin in xenografts.
  • These results together with the reduction of the expression of the colon cancer stem cell markersASCL2 andLGR5 (e.g., Hirschet al, 2013; Ziskinet al, 2013) raise the possibility of an inhibitory effect of Ivermectin, Selamectin and related macrocyclic lactones on TCF-dependent cancer stem cells.
  • the capacity of cancer cells to form 3D spheroids in culture, as well as the growth of these, is also WNT-TCF-dependent (Kanwaret al, 2010) and they were also affected by Ivermectin treatment
  • If Ivermectin is specific, it should only block TCF-dependent tumor growth. Indeed, the sensitivity and insensitivity of DLD1 and CC14 xenografts to Ivermectin treatment, respectively, together with the desensitization to Ivermectin actionin vivo by constitutively active TCF provide evidence of the specificity of this drug to block an activated WNT-TCF pathway in human cancer.
  • Ivermectin has a good safety profile since onlyin-vivo-dnTCF-sensitive cancer xenografts are responsive to Ivermectin treatment, and we have not detected side effects in Ivermectin-treated mice at the doses used
  • previous work has shown that side effects from systemic treatments with clinically relevant doses in humans are rare (Yang, 2012), that birth defects were not observed after exposure of pregnant mothers (Pacquéet al, 1990) and that this drug does not cross the blood–brain barrier (Kokozet al, 1999). Similarly, only dogs with mutantABCB1 (MDR1) alleles leading to a broken blood–brain barrier show Ivermectin neurotoxicity (Mealeyet al, 2001; Orzechowskiet al, 2012)
  • Indications may include treatment for incurable β-CATENIN/TCF-dependent advanced and metastatic human tumors of the lung, colon, endometrium, and other organs.
  • Ivermectin, Selamectin, or related macrocyclic lactones could also serve as topical agents for WNT-TCF-dependent skin lesions and tumors such as basal cell carcinomas
  • they might also be useful as routine prophylactic agents, for instance against nascent TCF-dependent intestinal tumors in patients with familial polyposis and against nascent sporadic colon tumors in the general aging population
  • Nathan Goodyear on 19 Mar 18
     
    Ivermectin, a common anti-parasitic, found to inhibit WTF-TCF pathway and decrease c-terminal phosophorylaiton of Beta-CATENIN all resulting in increased aptosis and inhibition of cancer growth in colon cancer cell lines and lung cancer cell lines.
fnfdoc

Types Causes And Symptoms Of Brain Tumor | Your Health Our Priority - 0 views

www.fnfdoc.com/...es-causes-symptoms-brain-tumor

Brain Tumor Glial Cells Health Types Of

shared by fnfdoc on 28 Apr 18 - No Cached
  • fnfdoc on 28 Apr 18
     
    Brain Tumor risks including surgery facts, as well as diagnosis also types either the primary tumor or secondary tumor. Treatments like MRI CT scan helping you to decide better for your health.
Nathan Goodyear

From the Cover: Pharmacologic doses of ascorbate act as a prooxidant and decrease growt... - 0 views

www.ncbi.nlm.nih.gov/...PMC2516281

cancer IV intravenous vitamin C IV vitamin C

shared by Nathan Goodyear on 18 Sep 13 - No Cached
  • An extensive panel of 43 tumor and 5 normal cell lines were exposed to ascorbate in vitro for ≤2 h to mimic clinical pharmacokinetics
  • effective concentration that decreased survival 50% (EC50) was determined. EC50 was <10 mM for 75% of tumor cells tested, whereas cytotoxicity was not evident in normal cells with >20 mM ascorbate
  • The addition of catalase to the medium ameliorated death of ovarian carcinoma (Ovcar5), pancreatic carcinoma (Pan02), and glioblastoma (9L) cells exposed to 10 mM ascorbate (1 h), indicating cytotoxicity was mediated by H2O2
  • ...8 more annotations...
  • A treatment dose of 4 g ascorbate/kg body weight either once or twice daily did not produce any discernible adverse effects
  • Xenograft experiments showed that parenteral ascorbate as the only treatment significantly decreased both tumor growth and weight by 41–53%
  • Peak plasma concentrations of ascorbate approached 30 mM
  • Pharmacologic concentrations of ascorbate decreased tumor volumes 41–53% in diverse cancer types known for both their aggressive growth and limited treatment options.
  • Our findings showed that pharmacologic ascorbic acid concentrations were cytotoxic to many types of cancer cells in vitro (Fig. 1A) and significantly impeded tumor progression in vivo without toxicity to normal tissues
  • The amelioration of ascorbate cytotoxicity in vitro by the addition of catalase was consistent among sensitive cancer cells (Fig. 1B) and points unambiguously to H2O2 generation in the extracellular medium
  • the current in vivo data support that pharmacologic ascorbate concentrations, which can readily be achieved in humans (Fig. 3E), diminished growth of several aggressive cancer types in mice (Fig. 2) without causing apparent adverse effects.
  • These intratumoral H2O2 concentrations of >125 μM persisted for >3 h after ascorbate administration
  • Nathan Goodyear on 18 Sep 13
     
    Tumor xenograft model in mice finds reduction in growth rates of ovarian cancer, pancreatic cancer, and glioblastoma with daily IV vitamin C.
spineneuro

Affordable Cost of Brain Tumor Surgery India Will Increase Your Life Span - 0 views

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brain tumor surgery low cost of brain tumor surgery India's best brain tumor surgeons

shared by spineneuro on 28 Aug 22 - No Cached
  • spineneuro on 28 Aug 22
     
    India is well known globally for the low cost of brain tumor surgery India. India sees limitless patients coming from all parts of the world to get treated for brain tumors in the excellent way possible.
spineneuro

Brain Tumor Surgery Success Rate In India Offering With Hope - 0 views

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Brain Tumor Surgery Brain tumor surgery success rate in India brain tumor surgery cost in rupees

shared by spineneuro on 18 Sep 22 - No Cached
  • spineneuro on 18 Sep 22
     
    Brain tumor surgery success rate in India is the most effective and it targets the specific place and the cells, consequently, giving it the highest brain tumor surgery success rate in India.
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Top 10 Brain Specialist Doctor in World Perform First-in-India Robot-Assisted Neuro Sur... - 0 views

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Top 10 brain specialist doctors in World brain tumor surgeries Brain Tumor Surgery in India Brain Tumor Surgery

shared by spineneuro on 14 Dec 21 - No Cached
  • spineneuro on 14 Dec 21
     
    Top 10 brain specialist doctors in India conducted the world's first robot-assisted neurosurgery. They are one of the few surgeons within the world to discover a unique interest in complex brain tumor surgeries and have successfully operated on a large number of brain tumor patients. Brain Tumor Surgery in India International Helpline Number : +91-9325887033 Email id: enquiry@spineandneurosurgeryhospitalindia.com
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